Evidence map›Paper›PMID 26283684›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2016

EphA2 Expression Is a Key Driver of Migration and Invasion and a Poor Prognostic Marker in Colorectal Cancer.

Philip D Dunne, Sonali Dasgupta, Jaine K Blayney, Darragh G McArt, Keara L Redmond, Jessica-Anne Weir, Conor A Bradley, Takehiko Sasazuki, Senji Shirasawa, Tingting Wang and 7 more

Open access · greenAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
6.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

89 citing papers in PubMed, 138 citations in OpenAlex.

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29 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 3 countries.

Philip D Dunne *Centre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Sonali Dasgupta *Centre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Jaine K BlayneyCentre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Darragh G McArtCentre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Keara L RedmondCentre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Jessica-Anne WeirCentre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Conor A BradleyCentre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Takehiko SasazukiInstitute for Advanced Study, Kyushu University, Fukuoka 812-8582, Higashi-ku, Japan.
Senji ShirasawaDepartment of Cell Biology, Faculty of Medicine, Fukuoka University, Jonan-Ku, Fukuoka 814-0180, Japan.
Tingting WangCancer Science Institute of Singapore, National University of Singapore, Singapore.
Supriya SrivastavaCancer Science Institute of Singapore, National University of Singapore, Singapore.
Chee Wee OngCentre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Ken ArthurCentre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Manuel Salto-TellezCentre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Richard H WilsonCentre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Patrick G Johnston *Centre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Sandra Van Schaeybroeck *Centre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.
Queen's University Belfast · GBNational University of Singapore · SGFukuoka University · JPKyushu University · JP

Funding

Cancer Research UK 13172Cancer Research UK A13172Cancer Research UK A13721Cancer Research UK C13749/A7261Cancer Research UK C212/A7402
6 · The paper itself

Abstract

purposeEphA2, a member of the Eph receptor tyrosine kinases family, is an important regulator of tumor initiation, neovascularization, and metastasis in a wide range of epithelial and mesenchymal cancers; however, its role in colorectal cancer recurrence and progression is unclear. EXPERIMENTAL

designEphA2 expression was determined by immunohistochemistry in stage II/III colorectal tumors (N = 338), and findings correlated with clinical outcome. The correlation between EphA2 expression and stem cell markers CD44 and Lgr5 was examined. The role of EphA2 in migration/invasion was assessed using a panel of KRAS wild-type (WT) and mutant (MT) parental and invasive colorectal cancer cell line models.

resultsColorectal tumors displayed significantly higher expression levels of EphA2 compared with matched normal tissue, which positively correlated with high CD44 and Lgr5 expression levels. Moreover, high EphA2 mRNA and protein expression were found to be associated with poor overall survival in stage II/III colorectal cancer tissues, in both univariate and multivariate analyses. Preclinically, we found that EphA2 was highly expressed in KRASMT colorectal cancer cells and that EphA2 levels are regulated by the KRAS-driven MAPK and RalGDS-RalA pathways. Moreover, EphA2 levels were elevated in several invasive daughter cell lines, and downregulation of EphA2 using RNAi or recombinant EFNA1 suppressed migration and invasion of KRASMT colorectal cancer cells.

conclusionsThese data show that EpHA2 is a poor prognostic marker in stage II/III colorectal cancer, which may be due to its ability to promote cell migration and invasion, providing support for the further investigation of EphA2 as a novel prognostic biomarker and therapeutic target.

Indexed as

Gene ExpressionBiomarkers, TumorCell Line, TumorCell MovementColorectal NeoplasmsHumansKaplan-Meier EstimateNeoplasm InvasivenessNeoplasm StagingPrognosisProportional Hazards ModelsProto-Oncogene Proteins p21(ras)ral GTP-Binding Proteinsral Guanine Nucleotide Exchange Factorras ProteinsReceptor, EphA2Biomarkers, TumorKRAS protein, humanProto-Oncogene Proteins p21(ras)ral GTP-Binding Proteinsral Guanine Nucleotide Exchange Factorras ProteinsReceptor, EphA2

Identifiers

PMID26283684
PMCPMC4694030
OpenAlexW2134642258

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.